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首页> 外文期刊>Molecular biology of the cell >Plk1 regulates activation of the anaphase promoting complex by phosphorylating and triggering SCF beta TrCP-dependent destruction of the APC inhibitor Emi1
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Plk1 regulates activation of the anaphase promoting complex by phosphorylating and triggering SCF beta TrCP-dependent destruction of the APC inhibitor Emi1

机译：Plk1通过磷酸化和触发APC抑制剂Emi1的SCFβTrCP依赖性破坏来调节后期促进复合物的活化

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摘要

Progression through mitosis requires activation of cyclin B/Cdk1 and its downstream targets, including Polo-like kinase and the anaphase-promoting complex (APC), the ubiquitin ligase directing degradation of cyclins A and B. Recent evidence shows that APC activation requires destruction of the APC inhibitor Emi1. In prophase, phosphorylation of Emi1 generates a D-pS-G-X-X-pS degron to recruit the SCFbetaTrCP ubiquitin ligase, causing Emi1 destruction and allowing progression beyond prometaphase, but the kinases directing this phosphorylation remain undefined. We show here that the polo-like kinase Plk1 is strictly required for Emi1 destruction and that overexpression of Plkl is sufficient to trigger Emi1 destruction. Plkl stimulates Emi1 phosphorylation, betaTrCP binding, and ubiquitination in vitro and cyclin B/Cdk1 enhances these effects. Plkl binds to Emi1 in mitosis and the two proteins colocalize on the mitotic spindle poles, suggesting that Plkl may spatially control Emi1 destruction. These data support the hypothesis that Plkl activates the APC by directing the SCF-dependent destruction of Emi1 in prophase.
机译：通过有丝分裂进展需要激活细胞周期蛋白B / Cdk1及其下游靶标，包括Polo样激酶和后期促进复合物（APC），泛素连接酶指导细胞周期蛋白A和B降解。最近的证据表明，APC激活需要破坏细胞周期蛋白B / Cdk1。 APC抑制剂Emi1。在前期，Emi1的磷酸化会产生D-pS-G-X-X-pS degron，以募集SCFbetaTrCP泛素连接酶，引起Emi1破坏并允许超过前中期的进程，但指导该磷酸化的激酶仍然不确定。我们在这里显示，Polol激酶Plk1是Emi1破坏的严格要求，而Plkl的过度表达足以触发Emi1破坏。 Plk1在体外刺激Emi1磷酸化，betaTrCP结合和泛素化，而细胞周期蛋白B / Cdk1增强这些作用。 Plk1在有丝分裂中与Emi1结合，并且这两个蛋白共定位在有丝分裂纺锤体的两极上，这表明Plk1可能在空间上控制Emi1的破坏。这些数据支持以下假设：Plk1通过指导前期Emi1的SCF依赖性破坏来激活APC。

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